Cigarette smoke gas phase induces ferroptosis via PKCβ in J774 macrophages

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  • タバコ煙ガス相はJ774マクロファージにおいてPKCβを介してフェロトーシスを誘導する

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<p>Cigarette smoking is a risk factor for various types of diseases including atherosclerosis, hypertension, chronic obstructive pulmonary disease, and respiratory infection. The respiratory infection caused by cigarette smoking is due to immune cell dysfunction by cigarette smoke, although its molecular mechanism remains to be clarified. The cigarette smoke can be divided into two phases: tar (particle) phase and gas phase. We have previously reported that gas phase extract of cigarette smoke (CSE) induces cell death. In this study, we have examined the effects of CSE on J774 macrophages. CSE and unsaturated carbonyl compounds, cytotoxic factors in the CSE, induced cell death in J774 macrophages. Ferrostatin-1 and liproxstatin-1, ferroptosis inhibitors, suppressed cell death caused by CSE and unsaturated carbonyl compounds. A broad-range protein kinase C (PKC) inhibitor Gö6983 suppressed CSE- and unsaturated carbonyl compounds-induced cell death. To identify PKC isoforms involved in the process, we have examined isoform-specific inhibitors. Enzastaurin, a PKCβ-specific inhibitor, suppressed the cell death. Enzastaurin also suppressed RSL3-induced ferroptosis. These results suggest that CSE and unsaturated carbonyl compounds induce PKCβ-dependent ferroptosis in J774 macrophages.</p>

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